| Co-Investigator(Kenkyū-buntansha) |
YAGI Takasi 大阪府立大学, 産学官連携機構, 教授 (80182301)
TAUCHI Hiroshi 茨城大学, 理学部, 教授 (70216597)
KATO Akihiro 京都大学, 放射線生物研究センター, 研究員 (70423051)
MORISIMA Kenichi 広島大学, 原爆放射線医科学研究所, 助教 (00363078)
MATSUURA Shinya 広島大学, 原爆放射線医科学研究所, 教授 (90274133)
槌田 謙 (槌田 健) 京都大学, 放射線生物研究センター, 研究員 (80397570)
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| Budget Amount *help |
¥108,680,000 (Direct Cost: ¥83,600,000、Indirect Cost: ¥25,080,000)
Fiscal Year 2010: ¥15,990,000 (Direct Cost: ¥12,300,000、Indirect Cost: ¥3,690,000)
Fiscal Year 2009: ¥19,760,000 (Direct Cost: ¥15,200,000、Indirect Cost: ¥4,560,000)
Fiscal Year 2008: ¥19,760,000 (Direct Cost: ¥15,200,000、Indirect Cost: ¥4,560,000)
Fiscal Year 2007: ¥24,570,000 (Direct Cost: ¥18,900,000、Indirect Cost: ¥5,670,000)
Fiscal Year 2006: ¥28,600,000 (Direct Cost: ¥22,000,000、Indirect Cost: ¥6,600,000)
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| Research Abstract |
By using phosphorylation of histone H2AX as a marker of DNA lesion, we showed here that DNA double strand breaks were generated by several environmental genotoxic and carcinogenic agents including UV and DNA cross-linking agents. These agents also induced gene mutations through translesional DNA synthesis, which is associated with NBS1. NBS1 is also involved in phosphorylation of H2AX and chromatin-remodeling at sites of DNA damage. Thus, NBS1 plays important roles in genome stability (inhibition of tumorigenesis) through DNA repair and cellular response to DNA lesions.
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